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Updated: Sep 23, 2025

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
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Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

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The E3 Ubiquitin Ligase Fbxo4 Functions as a Tumor Suppressor: Its Biological Importance and Therapeutic Perspectives

Shuo Qie1,2,3,4

  • 1Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Huanhuxi Road, Tiyuanbei, Hexi District, Tianjin 300060, China.

Cancers
|May 14, 2022
PubMed

Insights

Fbxo4 is an F-box protein that acts as a tumor suppressor by regulating cell cycle and proliferation. Its functions suggest potential for targeted cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Fbxo4 (F-box protein 4) is part of the F-box protein family, crucial components of SCF ubiquitin ligase complexes.
  • It interacts with Skp1 and Cullin1 to mediate substrate ubiquitination and degradation.
  • Dysregulation of Fbxo4 is implicated in various cellular processes relevant to cancer.

Purpose of the Study:

  • To review the structure, regulation, and function of Fbxo4.
  • To identify Fbxo4 substrates and their roles in cancer.
  • To explore the therapeutic potential of Fbxo4 in oncology.

Main Methods:

  • Literature review of studies on Fbxo4.
  • Analysis of Fbxo4's interaction partners and substrates.
  • Examination of Fbxo4's role in cell cycle, proliferation, apoptosis, and migration.

Main Results:

  • Fbxo4 targets proteins such as cyclin D1, p53, and Mcl-1, influencing cell cycle and apoptosis.
  • Fbxo4 exhibits tumor suppressor activities by regulating oncogenic pathways.
  • Its substrates are involved in critical cellular functions, including proliferation and invasion.

Conclusions:

  • Fbxo4 plays a significant role as a tumor suppressor in human cancers.
  • Understanding Fbxo4's mechanisms provides insights into cancer development.
  • Fbxo4 represents a promising target for novel cancer therapies.
Keywords:
DNA damage responseFbxo4Fxr1Trf1cell cyclecellular senescencecyclin D1metabolic reprogrammingtumor development and progression

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